ライフサイエンスコーパス: castration

1 n tumors after androgen deprivation therapy (castration).

2 Moreover, phospho-Akt remained high after castration.

3 nts no longer respond to medical or surgical castration.

4 androgen-intact mice and in tumors surviving castration.

5 ne expression patterns normally decreased by castration.

6 Moreover, castration also yields similar neuroprotective benefits

7 ive androgen-deprivation therapy by surgical castration and those who receive gonadotropin-releasing

8 endered susceptible to liver inflammation by castration, and testosterone treatment was sufficient to

9 Castration blunted androgen-mediated Cyp4a12 synthesis a

10 hese phenotypes were sharply abrogated after castration but restored with exogenous testosterone, sug

11 nd significantly prolongs survival following castration by enhancing p53 and androgen receptor acetyl

12 ssion is related to sexual hormones, as male castration decreased AIRE thymic expression and estrogen

13 Moreover, castration diminished male ventricular Kcne4 expression

14 e pigs, one of the alternatives for surgical castration, entails the possible occurrence of boar tain

15 Cixutumumab was synergistic with castration in a hormone-sensitive prostate cancer xenogr

16 lls was sufficient to restore sensitivity to castration in a mouse xenograft model system.

17 l castration is equally effective as medical castration in controlling prostate cancer (PCa).

18 n-deprivation therapy (ADT) through surgical castration is equally effective as medical castration in

19 ed expansion of Foxn1(+)Ly51(+)CD80(-) TECs, castration led to expansion of Foxn1(+)Ly51(-)CD80(+) TE

20 ion is rapidly elevated in the prostate upon castration-mediated androgen withdrawal through an undef

21 erapies for advanced prostate cancer include castration modalities that suppress ligand-dependent tra

22 Prostate cancer resistance to castration occurs because tumours acquire the metabolic

23 Castration of conditional Pten knock-out mice showed inc

24 While castration of dystrophin and utrophin double mutant (mdx

25 Surgical castration of male pigs will soon be abandoned, turning

26 Castration of male Prkca(-/-) but not WT mice results in

27 While castration of mdx-dm mice resulted in weaker muscle and

28 and its level is significantly elevated upon castration of mice carrying xenograft prostate tumors.

29 We demonstrate that prepubescent castration of Scly(-/-)Sepp1(-/-) mice prevents behavior

30 Castration of the above transgenic mice resulted in sign

31 s sexual dimorphism, as ovariectomy, but not castration, of Nf1-OPG mice normalizes RGC survival and

32 that blockade of AR signaling either through castration or AR-antagonist prevented and reversed cardi

33 tantly, LBH589 treatment in combination with castration prevents mCRPC development and significantly

34 Herein, we report that prepubescent castration provides neuroprotection by increasing seleni

35 ride in patients with bone metastases due to castration-refractory prostate cancer.

36 for neuroendocrine neoplasms and metastatic castration-refractory prostate cancer.

37 view is to summarize molecular mechanisms of castration resistance and provide an update in the devel

38 ght into the bona fide mechanisms underlying castration resistance and provide the foundation for the

39 tor (AR) transcriptional programs, including castration resistance and subsequent chromosomal translo

40 onally impair HR prior to the development of castration resistance and that, this potentially could b

41 xpression of PCGEM1 and AR3, contributing to castration resistance in prostate cancer.

42 nsensitive state in vitro, and YAP conferred castration resistance in vivo.

43 Castration resistance involves reactivation of androgen

44 In prostate cancer, the development of castration resistance is pivotal in progression to aggre

45 anding the disease biology and mechanisms of castration resistance led to significant advancements an

46 ed in the development of bone metastasis and castration resistance of prostate cancer.

47 Tumors in which castration resistance was conferred by NEK6 were predomi

48 While the time to develop castration resistance was similar in both subgroups, the

49 survival, progression-free survival, time to castration resistance, skeletal-related events, and adve

50 to the identification of known mediators of castration resistance, which served to validate the scre

51 t AR3 which has been shown to play a role in castration resistance.

52 s lost during prostate cancer progression to castration resistance.

53 , chromatin landscape, and leads to relative castration resistance.

54 (PCa) development and progression, including castration resistance.

55 Castration-resistance prostate cancer (CRPC), also known

56 dicating this population eventually leads to castration-resistance, owing to the continued survival o

57 ed phase II clinical development in men with castration resistant (advanced) prostate cancer (CRPC).

58 tive prostate cancer typically progresses to castration resistant prostate cancer (CRPC) after the an

59 5alpha-dihydrotestosterone, respectively, in castration resistant prostate cancer (CRPC).

60 axis regulates multiple oncogenic drivers of castration resistant prostate cancer (CRPC).

61 docetaxel cycles in patients with metastatic castration resistant prostate cancer (mCPRC) has not bee

62 widely used drug in patients with metastatic castration resistant prostate cancer (mCRPC).

63 er, but almost all cancer eventually becomes castration resistant, and the underlying mechanisms are

64 Castration-resistant (CR) prostate cancer (PCa) partly a

65 for the progression of prostate cancer to a castration-resistant (CRPC) state.

66 profile is enriched in advanced, anaplastic, castration-resistant and metastatic prostate cancers.

67 n with advanced PC (proven metastatic and/or castration-resistant biochemical progression) were rando

68 We employ lineage tracing to show that these castration-resistant Bmi1-expressing cells (or CARBs) ar

69 Silencing NEK6 in castration-resistant cancer cells was sufficient to rest

70 at advanced stages including metastatic and castration-resistant cancer remains incurable due to the

71 Castration-resistant cancers contained a higher percenta

72 ficantly elevated in primary PC samples from castration-resistant compared with therapy-naive patient

73 ostate cancers, but effective treatments for castration-resistant disease remain elusive.

74 ic treatment in patients with metastatic and castration-resistant disease.

75 cts, alters quality of life, and may lead to castration-resistant disease.

76 plice variants (AR-SV)-driven advanced stage castration-resistant disease.

77 Eventually the disease changes into a castration-resistant form of PCa where LBD mutations ren

78 prostate cancer cell motility, invasion, and castration-resistant growth and as a potential therapeut

79 mi1 as a marker for a distinct population of castration-resistant luminal epithelial cells enriched i

80 repressor protein Bmi1 marks a population of castration-resistant luminal epithelial cells enriched i

81 receptor acetylation and in turn sensitizing castration-resistant mesenchymal-like tumor cells to and

82 stinct from the previously described luminal castration-resistant Nkx3.1-expressing cells (CARNs).

83 ly labels a type of luminal stem cells named castration-resistant Nkx3.1-expressing cells (CARNs).

84 he maintenance of daughter cells produced by castration-resistant Nkx3.1-expressing luminal stem cell

85 societies, and those who develop metastatic castration-resistant PC (CRPC) invariably succumb to the

86 as well as a dramatic response of metastatic castration-resistant PC after PSMA radioligand therapy.

87 Data from 45 patients with castration-resistant PC and bone metastases during (223)

88 the upregulation of AR protein expression in castration-resistant PC.

89 e potential to expand options for metastatic castration-resistant PC.

90 protein levels increase with progression to castration-resistant PCa (CRPC) and high levels of Bag-1

91 ckdown occurs in both androgen-dependent and castration-resistant PCa (CRPC) cells, although the effe

92 r (PCa) in many countries, but its effect on castration-resistant PCa (CRPC) is limited.

93 rivation therapy, however, PCa progresses to castration-resistant PCa (CRPC), making the development

94 pression is markedly decreased in metastatic castration-resistant PCa (mCRPC) samples.

95 es the growth of both androgen-dependent and castration-resistant PCa xenografts.

96 was moderate to test all men with metastatic castration-resistant PCA, regardless of family history,

97 apies have gained attention as adjuvants for castration-resistant PCa.

98 1 inhibition via shRNA or PX-12 reverses the castration-resistant phenotype of CRPC cells, significan

99 The transition from castration-resistant prostate adenocarcinoma (CRPC) to n

100 The precise molecular alterations driving castration-resistant prostate cancer (CRPC) are not clea

101 or, improves survival in men with metastatic castration-resistant prostate cancer (CRPC) before and a

102 ndrogen-dependent prostate cancer (ADPC) and castration-resistant prostate cancer (CRPC) cell lines,

103 rapies have significantly improved survival, castration-resistant prostate cancer (CRPC) cells are ev

104 Finally, androgen-independent AR activity in castration-resistant prostate cancer (CRPC) cells is dri

105 environment, have created the need to revise castration-resistant prostate cancer (CRPC) clinical tri

106 Castration-resistant prostate cancer (CRPC) continues to

107 Patients with metastatic castration-resistant prostate cancer (CRPC) frequently d

108 The view of castration-resistant prostate cancer (CRPC) has changed

109 Men who develop metastatic castration-resistant prostate cancer (CRPC) invariably s

110 The development of castration-resistant prostate cancer (CRPC) is associate

111 Castration-resistant prostate cancer (CRPC) is character

112 The lethal phenotype of castration-resistant prostate cancer (CRPC) is generally

113 Castration-resistant prostate cancer (CRPC) is the letha

114 Castration-resistant prostate cancer (CRPC) is the main

115 Metastatic castration-resistant prostate cancer (CRPC) is the prima

116 Trials in castration-resistant prostate cancer (CRPC) need new cli

117 nce of prostate cancer either in the form of castration-resistant prostate cancer (CRPC) or transdiff

118 used clinical tissue from lethal metastatic castration-resistant prostate cancer (CRPC) patients obt

119 Castration-resistant prostate cancer (CRPC) remains a ma

120 ntinues to have a critical role in promoting castration-resistant prostate cancer (CRPC) survival and

121 the progression of prostate cancer (PCa) and castration-resistant prostate cancer (CRPC) through upre

122 rk [ACRIN] 6687) to a multicenter metastatic castration-resistant prostate cancer (CRPC) tissue bioma

123 ough initially effective, leads to incurable castration-resistant prostate cancer (CRPC) via compensa

124 circulating tumor cells (CTCs) from men with castration-resistant prostate cancer (CRPC) was associat

125 onal therapy for chemotherapy-naive men with castration-resistant prostate cancer (CRPC) who range fr

126 s the first therapeutic approach in treating castration-resistant prostate cancer (CRPC), but tumours

127 efficacy and promotes progression to lethal castration-resistant prostate cancer (CRPC), even when p

128 ing tumors, most patients eventually develop castration-resistant prostate cancer (CRPC), for which t

129 (LBD) are associated with the development of castration-resistant prostate cancer (CRPC), including r

130 articularly virulent form of this disease is castration-resistant prostate cancer (CRPC), where patie

131 o remission, the disease often progresses to castration-resistant prostate cancer (CRPC), which is st

132 and PPP3CC is formed during the emergence of castration-resistant prostate cancer (CRPC).

133 is overexpressed and hyperactivated in human castration-resistant prostate cancer (CRPC).

134 o detect metastatic hormone-naive (HNPC) and castration-resistant prostate cancer (CRPC).

135 evelopment of novel treatment strategies for castration-resistant prostate cancer (CRPC).

136 inevitably relapses and progresses to lethal castration-resistant prostate cancer (CRPC).

137 potential therapeutic target for metastatic castration-resistant prostate cancer (CRPC).

138 of the predominantly upregulated pathways in castration-resistant prostate cancer (CRPC).

139 biraterone and enzalutamide in patients with castration-resistant prostate cancer (CRPC).

140 receptor (AR) activity are major drivers of castration-resistant prostate cancer (CRPC).

141 approval of abiraterone for the treatment of castration-resistant prostate cancer (CRPC).

142 patients will relapse and develop incurable castration-resistant prostate cancer (CRPC).

143 a phase II nonrandomized expansion study in castration-resistant prostate cancer (CRPC).

144 genic pathways that contribute to metastatic castration-resistant prostate cancer (CRPC).

145 s receiving ADT eventually develop incurable castration-resistant prostate cancer (CRPC).

146 cancer deaths due to disease progression to castration-resistant prostate cancer (CRPC).

147 rapy failure leads to terminal and incurable castration-resistant prostate cancer (CRPC).

148 I]) in patients who have advanced metastatic castration-resistant prostate cancer (mCRPC) and are rec

149 l-related events in patients with metastatic castration-resistant prostate cancer (mCRPC) and bone me

150 established prognostic factors in metastatic castration-resistant prostate cancer (mCRPC) and the ass

151 o androgen receptor inhibition in metastatic castration-resistant prostate cancer (mCRPC) and whether

152 clear medicine is theranostics of metastatic castration-resistant prostate cancer (mCRPC) based on mo

153 ist enzalutamide in patients with metastatic castration-resistant prostate cancer (mCRPC) is undefine

154 cal decision in the management of metastatic castration-resistant prostate cancer (mCRPC) is when to

155 tumor cells (CTC) from 179 unique metastatic castration-resistant prostate cancer (mCRPC) patients to

156 Whole-exome sequencing of metastatic castration-resistant prostate cancer (mCRPC) reveals tha

157 rogression-free survival (PFS) in metastatic castration-resistant prostate cancer (mCRPC) trials has

158 d Methods Fifty-six patients with metastatic castration-resistant prostate cancer (mCRPC) with osseou

159 Purpose In patients with metastatic castration-resistant prostate cancer (mCRPC), overall su

160 precision medicine framework for metastatic, castration-resistant prostate cancer (mCRPC), we establi

161 -mesenchymal transition (EMT) and metastatic castration-resistant prostate cancer (mCRPC), which is c

162 get for radionuclide therapy of metastasized castration-resistant prostate cancer (mCRPC).

163 ty in men with previously treated metastatic castration-resistant prostate cancer (mCRPC).

164 rolled phase II trial in men with metastatic castration-resistant prostate cancer (mCRPC).

165 n a large cohort of patients with metastatic castration-resistant prostate cancer (mCRPC).

166 ) ((177)Lu-PSMA) in patients with metastatic castration-resistant prostate cancer (mCRPC).

167 g resistance mechanism to anti-AR therapy in castration-resistant prostate cancer (mCRPC).

168 ses to treatment in patients with metastatic castration-resistant prostate cancer (mCRPC).

169 lly significant co-occurrences in metastatic castration-resistant prostate cancer (mCRPC).

170 relentless progression to lethal metastatic castration-resistant prostate cancer (mCRPC).

171 nd therapy (RLT) of patients with metastatic castration-resistant prostate cancer (mCRPC).

172 s), and subsequent progression to metastatic castration-resistant prostate cancer (mCRPC).

173 The processes associated with transition to castration-resistant prostate cancer (PC) growth are not

174 ly clinical development for the treatment of castration-resistant prostate cancer (PCa).

175 esponses in asymptomatic men with metastatic castration-resistant prostate cancer and also resensitis

176 le for participation if they had: metastatic castration-resistant prostate cancer and had received no

177 ely active in several malignancies including castration-resistant prostate cancer and has been identi

178 ional program in both androgen-sensitive and castration-resistant prostate cancer and inhibited tumou

179 rs are available to predict the emergence of castration-resistant prostate cancer and no curative opt

180 cruited patients with progressive metastatic castration-resistant prostate cancer and no previous che

181 sly reported ALSYMPCA trial in patients with castration-resistant prostate cancer and symptomatic bon

182 ffective and well tolerated in patients with castration-resistant prostate cancer and symptomatic bon

183 en receptor-regulated miRNA overexpressed in castration-resistant prostate cancer and that miR-32 can

184 role for BAT in the management of metastatic castration-resistant prostate cancer and the optimal str

185 validate the activation function of EZH2 in castration-resistant prostate cancer and to (ii) study t

186 It occurred in both androgen-dependent and castration-resistant prostate cancer and was associated

187 us prednisone in men with chemotherapy-naive castration-resistant prostate cancer at the interim anal

188 (1245A>C) has been mechanistically linked to castration-resistant prostate cancer because it encodes

189 a-118b, a patient-derived xenograft (PDX) of castration-resistant prostate cancer bone metastasis tha

190 tion of survival in patients with metastatic castration-resistant prostate cancer but also engage a c

191 ive and an androgen-independent mechanism in castration-resistant prostate cancer cells.

192 occur early are an unmet need in metastatic castration-resistant prostate cancer clinical research a

193 sponse end points for early-phase metastatic castration-resistant prostate cancer clinical trials.

194 Proteomic analysis of castration-resistant prostate cancer demonstrated the en

195 y androgen biosynthetic enzyme implicated in castration-resistant prostate cancer development.

196 Patients with metastatic castration-resistant prostate cancer have few treatment

197 rovements to prognostic models in metastatic castration-resistant prostate cancer have the potential

198 y-naive patients with progressive metastatic castration-resistant prostate cancer in a 1:1 ratio to r

199 hat prolongs survival in men with metastatic castration-resistant prostate cancer in whom the disease

200 ion of patients for a specific treatment for castration-resistant prostate cancer or the best sequenc

201 PET/CT in the prediction of survival in both castration-resistant prostate cancer patients and hormon

202 e PET/CT as a diagnostic tool for monitoring castration-resistant prostate cancer patients treated wi

203 Thirty-five castration-resistant prostate cancer patients with multi

204 iation therapy in advanced-stage, metastatic castration-resistant prostate cancer patients with prost

205 te cancer cell lines and cfDNA obtained from castration-resistant prostate cancer patients.

206 overall survival in patients with metastatic castration-resistant prostate cancer previously treated

207 raterone acetate in patients with metastatic castration-resistant prostate cancer progressing after c

208 tandard of care for patients with metastatic castration-resistant prostate cancer progressing after d

209 We enrolled patients who had metastatic castration-resistant prostate cancer progressing after t

210 ults show nelfinavir and its analogs inhibit castration-resistant prostate cancer proliferation by bl

211 1GSC treatments in mouse xenograft models of castration-resistant prostate cancer resulted in signifi

212 with radiographically documented metastatic castration-resistant prostate cancer that had progressed

213 is approved for the treatment of metastatic castration-resistant prostate cancer that has progressed

214 amined orteronel in patients with metastatic castration-resistant prostate cancer that progressed aft

215 to evaluate BAT in patients with metastatic castration-resistant prostate cancer that progressed aft

216 proteolysis as novel therapeutic targets for castration-resistant prostate cancer therapeutics.

217 nhibit proliferation and induce apoptosis of castration-resistant prostate cancer through inhibition

218 ses are highly expressed in human metastatic castration-resistant prostate cancer tissues.

219 t randomised clinical trials with metastatic castration-resistant prostate cancer to estimate the gro

220 gen and antiandrogen therapies in metastatic castration-resistant prostate cancer to maximise therape

221 ficantly longer for patients with metastatic castration-resistant prostate cancer treated with this c

222 e 3 clinical trials in first-line metastatic castration-resistant prostate cancer were obtained from

223 e 2 trial in which patients with metastatic, castration-resistant prostate cancer were treated with o

224 USE M1-in which 266 patients with metastatic castration-resistant prostate cancer were treated with p

225 uctive tract tissues and at higher levels in castration-resistant prostate cancer where it is require

226 d no survival benefit in men with metastatic castration-resistant prostate cancer with the addition o

227 rmed progressive bone-predominant metastatic castration-resistant prostate cancer with two or more sk

228 patients with chemotherapy-naive metastatic castration-resistant prostate cancer without visceral me

229 ditional cohorts (post-abiraterone and newly castration-resistant prostate cancer) are ongoing.

230 progressing on androgen-deprivation therapy (castration-resistant prostate cancer) has improved subst

231 th metastatic breast and six with metastatic castration-resistant prostate cancer, isolated via CellS

232 chemotherapy-naive patients with metastatic castration-resistant prostate cancer, radiographic progr

233 hesis and prolongs survival in patients with castration-resistant prostate cancer, which is otherwise

234 d and radiographically documented metastatic castration-resistant prostate cancer, with no more than

235 ion that provided new insights in metastatic castration-resistant prostate cancer.

236 3 is a potential target for the treatment of castration-resistant prostate cancer.

237 and is approved for patients with metastatic castration-resistant prostate cancer.

238 in men with chemotherapy-naive, metastatic, castration-resistant prostate cancer.

239 1, 2009, and July 31, 2013, with metastatic castration-resistant prostate cancer.

240 d not improve OS in patients with metastatic castration-resistant prostate cancer.

241 to licensing for the treatment of metastatic castration-resistant prostate cancer.

242 nt further studies of 6 for the treatment of castration-resistant prostate cancer.

243 ion that provided new insights in metastatic castration-resistant prostate cancer.

244 symptomatic or mildly symptomatic metastatic castration-resistant prostate cancer.

245 tandard of care for patients with metastatic castration-resistant prostate cancer.

246 e therapy response and prognosis in men with castration-resistant prostate cancer.

247 ith bicalutamide in patients with metastatic castration-resistant prostate cancer.

248 only agent with proven survival benefit for castration-resistant prostate cancer.

249 undergoing further development in metastatic castration-resistant prostate cancer.

250 chemotherapy-naive patients with metastatic castration-resistant prostate cancer.

251 nt in chemotherapy-naive men with metastatic castration-resistant prostate cancer.

252 tivity is the main driver for development of castration-resistant prostate cancer.

253 e treatment of androgen-sensitive as well as castration-resistant prostate cancer.

254 onal activity and promote the development of castration-resistant prostate cancer.

255 validated therapeutic target for metastatic castration-resistant prostate cancer.

256 o improvement in the treatment of metastatic castration-resistant prostate cancer.

257 patients with chemotherapy-naive metastatic castration-resistant prostate cancer.

258 chemotherapy-naive patients with metastatic castration-resistant prostate cancer.

259 tamide, a drug approved for the treatment of castration-resistant prostate cancer.

260 for chemotherapy-naive men with metastatic, castration-resistant prostate cancer.

261 navir or its analogs should be developed for castration-resistant prostate cancer.

262 chemotherapy-naive patients with metastatic castration-resistant prostate cancer.

263 AR output signature, is low in a portion of castration-resistant prostate cancer.

264 the androgen receptor and the development of castration-resistant prostate cancer.

265 clinical responses with ODM-201 in men with castration-resistant prostate cancer.

266 able to inhibit AR transactivation and treat castration-resistant prostate cancer.

267 sing direct STAT3 inhibitor for treatment of castration-resistant prostate cancer.

268 irst-line docetaxel treatment for metastatic castration-resistant prostate cancer.

269 the RLT and care of patients with metastatic castration-resistant prostate cancer.

270 P/p300 is required to maintain the growth of castration-resistant prostate cancer.

271 ith mitoxantrone in patients with metastatic castration-resistant prostate cancer.

272 overall survival in patients with metastatic castration-resistant prostate cancer.

273 erapeutic option in patients with metastatic castration-resistant prostate cancer.

274 rials that enrolled patients with metastatic castration-resistant prostate cancer.

275 6 signaling as a central mechanism mediating castration-resistant prostate cancer.

276 rivation therapy and in approximately 30% of castration-resistant prostate cancer.

277 CBP/p300 bromodomain as a strategy to treat castration-resistant prostate cancer.

278 Castration-resistant prostate cancers (CRPC) that arise

279 report that approximately 20% of metastatic castration-resistant prostate cancers express neither AR

280 Furthermore, androgen deprivation led to castration-resistant prostate cancers that were composed

281 We hypothesized that metastatic, castration-resistant prostate cancers with DNA-repair de

282 in human NEPC tumors compared to primary and castration-resistant prostate cancers, and its expressio

283 ate homologous recombination (HR) defects in castration-resistant prostate cancers, rendering these t

284 etastasis is the hallmark of progressive and castration-resistant prostate cancers.

285 llows functional substitution for AR in some castration-resistant prostate cancers.

286 t upregulation and hyperactivation of YAP in castration-resistant prostate tumors compared to their l

287 progression of androgen-dependent PCa to the castration-resistant stage.

288 d disease, tumors often progress to a lethal castration-resistant state (CRPC).

289 ocks AR signaling and inhibits the growth of castration-resistant tumors in vivo in mice.

290 Further evolution in castration-resistant tumors leads to tumors in which cel

291 observed substantial genomic overlap between castration-resistant tumors that were histologically cha

292 sly been implicated in the growth of NE-like castration-resistant tumors.

293 is independent of exogenous androgen in the castration-resistant variants of LNCaP, C4-2 and C4-2B.

294 y to the clinical CRPC, orthotopically grown castration-resistant VCaP (CR-VCaP) xenografts express h

295 tate cancer and inhibited tumour growth in a castration-resistant xenograft model.

296 Men with castration-sensitive prostate cancer and bone metastases

297 Additionally, we imaged one patient with castration-sensitive prostate cancer before and 4 wk aft

298 mouse xenograft model and in a patient with castration-sensitive prostate cancer.

299 gs can help clinicians decide on the optimal castration strategy for individual patients.

300 drogen action in the skin as demonstrated by castration studies and skin-specific androgen receptor d